"Biomechanics Corner": Overpronation

Re: Biomechanics Corner - Overpronation

do I get to join your side now please please.

When does pronation go from normal to hyper?

 

Re: Biomechanics Corner - Overpronation

Col,

My point was this; a patient presents in your clinic with PTTD and 'overpronation'. How can you possibly know if:

(A) His 'overpronation' led to a progressive increased work demand/overload of the Tibialis Posterior complex, i.e. his 'overpronation' caused his PTTD (via the tissue stress mechanism)?

(B) He had a Tibialis Posterior pathology initially, and as a consequence of its inability to exert supination moments across the STJ axis he developed a progressive flat foot deformity, i.e his PTTD caused his 'overpronation'?

This is the mistake people make when interpreting results from research with a cross sectional design - it shows a correlation but does not prove causation.

Do not forget this is another huge assumption on our part. Even if we leave the whole 'how much hyperpronation will cause alot of pathology' aside, we still have to remind ourselves that there is not a massive body evidence behind us to even suggest a pronated foot type causes pathology. Several prospective studies with ok methodology have concluded a pronated foot type is not predictive of future pathology.

I disagree - not saying it will be easy but this is where it is our job to educate. Not a single Physio I work with would ever say overpronation (infront of me anyway) as they know the look they'll get and the inevitable rant that follows. I'm still working on the Consultants...

Ian

 

Re: Biomechanics Corner - Overpronation

What we can say with confidence by using mechanical modelling techniques even though no cross-sectional research, or any other research for that matter, has necessarily supported all of these predictions:

1) Posterior tibial tendon dysfunction (PTTD) is caused by excessive tensile force within the posterior tibial tendon;

2) A foot with a medially deviated subtalar joint (STJ) axis will cause the posterior tibial muscle/tendon to have a reduced moment arm to cause internal STJ supination moment and will cause ground reaction force (GRF) to have an increased moment arm to cause external STJ pronation moment.

3) The reduced moment arm of the posterior tibial tendon, combined with the increased external STJ pronation moment from medial deviation of the STJ (see #2) will require increased tensile forces within the posterior tibial tendon to supinate the STJ during weightbearing activities.

4) Increased posterior tibial tension increases the risk of PTTD (see #1) and if posterior tibial muscle function is compromised as a result, will lead to decreased internal STJ supination moment and more liklihood of other anti-pronation structural components of the foot (e.g. spring ligament complex) being stretched, partially ruptured or completely ruptured due to increased tensile forces.

Sometimes, we must rely on our knowledge of physics and biomechanics and physiology of the human body, and not on available research specific to the pathology we are treating (since there often is none) to make the best treatment decisions for our patients in pain. Just because research hasn't shown it to be true, or research hasn't even been done to test whether it is true or not, doesn't mean it isn't so.

 

Hello

I read this post with interest, as it is obviously a hot topic and the “overponantion” idea has been talked about to the last degree. I do agree that the Sub Talar neutral is not a good starting point. However I think that a very important aspect is missing, if I could perhaps suggest that when assessing the range of movement of the foot on weight-bearing we do this in a “beach sand” box or similar method that allows the foot to position itself where the “foot” wants to be. That I believe is the neutral position for that foot and the starting point to assess the alignment of the rest of the body to determine the issue or issues that might be causing the injury. The fact that we walk on hard surfaces implies that our feet move into an unnatural pronated position. All the leading shoes shoe designers are moving towards designing shoes to allow “free foot” movement, this I believe is the way forward. However when running off road this is easier to achieve the “fee foot movement”. What happens when the feet start running on hard surfaces? This is the challenge that faces us, using this ethos; I believe the treatment protocol should look at guiding the foot and therefore the entire body into a position that is normal or neutral for that particular person. Using minor adjustments to the foot that realigns the foot during each phase from initial heel strike to toe off.

All the very best, hope to hear your thougts on this idea.

Gary

 

Hey Kevin.

Just so. Lack of evidence is not evidence of lack. And your description of the aetiology of PTTD is concise and logical as always.

However I do think Ian makes a good point in the sense of post hoc ergo propter hoc. A foot with a more medially deviated axis (which could be because of a more pronated functional range) could reasonably be expected to be at more risk of PTTD. However as you state in 4, PTTD could also be expected to be a risk factor for a more pronated foot.

Whilst it is certainly plausible that PTTD could be caused by a foot with a more pronated functional range, I do not think that to be the ONLY potential cause of PTTD.

For example, take a foot with a "normal" axial position and a "normal" range of pronation. Lets say they have an increasingly inefficient windlass, meaning the PTT has to do more, and has thus higher tensile stress. The PTT becomes less effective, the Deltoid complex stretches, the foot develops a lower pronatory range. Here now we have a foot with a medially deviated axis and increased pronation arising from PTTD rather than causing it.

Its a hair splitting pedantic and petty point, but I like those .

And in either case, "overpronation" is a pretty useless observation. Just to revert to the OP.

Regards
Robert

 

Hey Gary. Welcome to Pod Arena:welcome:

Hmmm. I don't think I've understood you here. It seems you suggest we take a weightbearing cast and take that as the desirable, or "normal" position. Leave alone the fact that the foot is not designed to function in any one position, how does this fit with the fact that our patients are all pathological.

Try this. You, in a wild rage at me for being a pedantic ass, fly to the uk and kick me really hard in the ankle, rupturing my medial ligaments (you brute). Over the next 2 months my ankle collapses completely leaving me walking on my navicular and with a functionally shorter limb causing a pelvic tilt etc etc. I fly out to you and demand you fix it, feeling slightly guilty you agree to do so. You take a weight bearing foam box cast and obviously my foot is pes pancakus. Is this its "normal or neutral position"?

Kind regards
Robert

 

Robert:

I never said that a medially deviated subtalar joint (STJ) axis is the only cause of posterior tibial tendon dysfunction (PTTD). However, I would bet that feet with preexisting medially deviated STJ axes are by far the most common cause of PTTD. Direct trauma to the posterior tibial tendon (such as contusions or lacerations) could also cause PTTD, but this is uncommon. And direct trauma to the posterior tibial tendon that causes PTTD, without a preexisting medially deviated STJ axis, I would call rare.

Since increased STJ pronation moments and lower medial longitudinal arch height are the normal cause of what you call "an increasing inefficient windlass" and since both increased STJ pronation moments and lower arch height are nearly always associated with medially deviated STJ axes, I find it difficult to understand how "an increasing inefficient windlass", as you say, can occur independent of changes in STJ spatial location. Maybe you can explain this further as to what "an increasing inefficient windlass" actually means.

I have written before on Podiatry Arena, on numerous occasions, that I believed the changes that occur in PTTD will occur simultaneously as I have described in this previous thread.

Therefore, while I would agree that PTTD can occur without a preexisting medially deviated STJ axis, my guess from treating probably over 1,000 cases of PTTD, is that PTTD only rarely occurs without a preexisting medially deviated STJ axis.

 

I can try...

Some clever bod gave a really good list of causes of fnHL on this forum ages back. I've tried to find the post but can't. One of them was

So perhaps a progressive bony change to the shape of the 1st met head could adversely affect the windlass.

I suspect if there was increasing structural HL due to OA that would render the windlass increasingly ineffective, to the point of hallux rigidus.

Kind regards
Robert

 

Robert:

So you are saying that a change in the shape of the 1st metatarsal head could cause posterior tibial tendon dysfunction?? Please explain the mechanism behind this.

 

I would think that if the windlass was exerting less supination moment one of three things would happen.

1. The foot would be in a more pronated position after heel lift

2. Other structures would generate more supination moment to compensate and the foot would be in the same position (but there would be more demand on the PTT)

3. A little of both.

I'm guessing for most people, at least initially, we would be looking at 2 or 3. In which case the PTT could have more demand placed on it, which if it cannot cope with will result in pathology.

This is going to come back to the old "FnHl causes pronation vs pronation causes FnHl" debate again isn't it...


Regards

 

Yes.:butcher:

 

Oh super.

Perhaps we should go back here

http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=3645

 

Yep.:butcher:

 

or here:
http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=1283
I think this is the publication of the study we were talking about in the above thread:
http://www.japmaonline.org/cgi/content/abstract/94/3/269

 

Well thats not at ALL intimidating!



Ok. Does or does not the plantarflexion of the 1st met after heel lift create supination moment.

 

How?

 

Got me thinking now (damn you). I was going to go for "increases GRF under 1st MH" but on reflection I think I prefer "raises base of 1st met relative to the heel and the ground". And although I do see plenty of feet with axes functioning medial to this point they rarely have a functioning windlass. But I could easily have got that well wrong.

My reasoning stems from observation rather than deduction. If I dorsiflex somebodies toe, they supinate, unless they have a knackered windlass. If I ask someone to stand on tiptoe, they supinate. When I watch them walk they supinate when they heel raise. When I look at the kinematics graph the supination almost all happens after heel lift.

Unless of course my friendly neighbourhood surgeon has been playing silly buggers with the 1st ray and the windlass no longer works. In which case none of the above happens. Except the graph. Obviously.

So go on then.

Blow a hole in my preconceptions again.

 

It's not about blowing holes in anyone's pre-conceptions, Robert. I was just trying to understand your point. I guess the next logical question is: how is the "base of 1st met raised relative to the heel and the ground"? i.e., how is this achieved? And moreover, how does raising the base of the met relative to the heel and the ground increase supination moment? Can you ignore the GRF beneath the metatarsal head btw?

Hint: think about the action of peroneus longus. Eric has written about this.

And I'm sorry to say this but: why do the windlasses rarely function in people with such medially deviated axes? QED, Robert.

 

Of course it is. If we can't critically examine our own beliefs how can we learn or progress? You know I love it.

trigonometry is it not? Shorten one side of the triangle and the opposite angle increases.

Whats proved, that a medially deviated axis causes increased internal plantarflexion moments in the 1st MPJ and that if the Internal plantarflexion moments exceed the external dorsiflexion moments the windlass can't function? Never disputed that for a second. But that was not the question.

My question remains. Irrespective of the whys and wherefors,

Regards

 

As you know Robert, it may or may not do depending upon the axial position of the STJ axis, among other things.

The point is that we have to look at the net effect in regard to your original hypothesis, that is both the internal and external moments being generated in this process. Hence my questions. So, you didn't really answer my question- how does raising the base of the first metatarsal increase STJ supination moment? And what about that external moment from GRF under the met head that you chose to disregard? And how does this relate to STJ axial position? Lets say we had an STJ axis that crossed from lateral to medial just proximal to the metatarsal head. Moreover, what structures generate these forces and what are the concomitant forces which they simultaneously generate?

QED, Robert? I agree, I can't see in your responses that "which was to be demonstrated", i.e. how an increase in the radius of curvature of the 1st metatarsal head causes tibialis posterior tendon dysfunction. Like I said, QED, Robert. Indeed, like you said, what has been proved? Certainly, Bart's study seems to support the hypothesis of pronation causing functional hallux limitus rather than vice versa- which if I am reading you correctly, remains your suggestion, despite that which has previously been demonstrated.

 

For what its worth here is what I really think tonight, increased GRF beneath the 1st met head resulting from 1st met plantarflexion should increase supination moment regardless of STJ axial position since even if the 1st met head is lateral to the STJ axis, the increased GRF here should draw the COP closer to the STJ axis- see the thread on forefoot valgus wedging. However, what we have to consider is that plantarflexion of the first ray is likely to occur in response to two main drivers: 1> peroneus longus contraction 2> compression on metatarsal head. Peroneus longus functions via a pulley mechanism about the cuboid, the action of peroneus longus at the cuboid will create internal pronation moment and external moment about the STJ axis; the nature of the external moment will depend upon the COP position and net GRF vector's relation to the STJ axial position. These moments about the STJ axis may or may not exceed the change brought about in external moment resulting from shift in COP due to increased GRF under the 1st met head due to 1st met plantarflexion. So the key is the STJ axial position. Something like that- it's late and I've had a tough day! Now, I'm just trying to work out how peroneus longus activity raises the base of the 1st metatarsal as Robert suggests. I can see how compression on the metatarsal via the base of the proximal phalanx could do this due to the inevitable force couple, I just can't see how peroneus longus can do this. Like I said, it's late and I'm tired- maybe tomorrow I'll have more lucid thoughts...... Without plantarflexion of the 1st met, can the windlass work so can we have adequate compression on the the 1st met head without windlass? I guess the ehl, fhl and intrinsics attaching to the hallux could achieve this in the absence of forces from the plantar fascia- rambling now.

 

Re: Biomechanics Corner - Overpronation

Thinking gobally you can add the CNS into the equation. When there is a high pronation moment from the ground there has to be a high supination moment from some source to counteract the pronation moment from the ground. The CNS is faced with some tough choices in the presence of a medially positoined STJ axis. It has to work that poor posterior tibial muscle and tendon much harder than feet with average STJ axes, or it can allow very high stresses in the anatomical structures that limit STJ pronation. If one of the structures becomes painful the options are worse.

I guess my point is the high tensile forces don't come from the ground, they come from high activation of the muscle from the CNS.

Cheers,

Eric

 

Don't think motion, think forces and moments. In a standing foot, the posterior tibial tendon tension increases, the STJ supinates, the medial arch rises and the ground reaction force decreases on the first met and the met plantar flexes. The met plantar flexion did not cause the supination moment.

Now to discuss moments at the STJ you should be talking about how forces get applied to the talus and the calcaneus. When you dorsiflex the 1st toe in stance the tension in the fascia increases and the first prox phalanx applies an anterior to posterior force on the metatarsal....then there is an anterior to posterior force from the navicular applied to the talar head at the same time there is an anterior pull at the plantar fascial attachment to the calcaneus. This will cause a supination moment most of the time.

These same forces that cause supination of the STJ will tend to cause plantar flexion of the metatarsal. The geometry is important, but it's the forces that do the work. See my Windlass paper.

Cheers,

Eric

 

If the first ray plantarflexes, and as a result the ground reaction force (GRF) is increased plantar to first metatarsal head as a result, then this will tend to either decrease the external STJ pronation moment or increase the external STJ supination moment, all other factors being equal. After heel off, probably a bigger factor than first ray plantarflexion in creating external STJ supination moment is the magnitude and duration of gastrocnemius-soleus contractile activity that creates an internal STJ supination moment.

 

I read this a couple of time and it starts to make sense. My question, how does this effect the MTJ . Ie as the PL contract there will be a increase in the external STJ supination moment ( from plantar to lat malleolar and cuboid) , Plantarflexion and increased stability of the 1st met. As the 1st met plantarflexes I´m thinking there will be an external inversion, dorsiflexion and abduction moments on the x,y,and z axis as discussed by nester.

If I´m correct in my thinking this will also have some effect on windlass and what happens at the STJ axis ? or maybe I´m just confused as I´m 2nd guessing my post now....

 

I released now how wrong my statement above was..


I clearing was not thinking thru this fully as the PL pull on the cuboid which is part of the MTJ.

Sorry for not thinking before writting. Bit of theme of my life... anyway.

why is it that we don´t discuss the MTJ . So the PL will effect the stj but it must be very effective on the mtj but in this case people are discussing 1st met, stj axis cop widlass etc but no mention of MTJ motion, moments etc.

 

Gosh what a lot of interesting stuff about the windlass! Thanks to Simon Kevin and Eric for taking the time.

Sorry Eric, Having a hard time with this. Bear with me.

Bit confused here. Are we talking about what happens at heel raise in gait? And if so have I correctly understood that you are saying the PT tension supinating the foot is what casues the 1st met to plantarflex rather than vice versa? and that this is different to what happens here

To return a few steps, and trying to keep it simple for simple folks like me...

Kevin Said

Thats what I thought.

So If the Windlass is inoperative (say bacause the 1st mpj cannot bend), is this supination moment lost?

I'm just trying to understand where in the chain of logic my dodgy link is.

The other thing I'd like to clarify is simons question on HOW the windlass exerts its supination moment. I think I understand the concept that there is force X + on the calc and X - on the base of the 1st at either end. I also understand that this will cause an increased GRF sub 1st met. Where I'm struggling is what happens next.

The downforce on the 1st met is transmitted from body weight which is exerted through the base of the 1st met. Is the counter force not also transferred throught the base of the 1st met?





Thanks
Robert

 

Robert:

In static stance, a flattened first metatarsal head, by itself, would have no net effect on STJ moments.

However, during walking, if the flattened first metatarsal head caused a restriction in 1st metatarsophalangeal joint (MPJ) dorsiflexion, then the individual has the option of, 1) not decreasing their duration of propulsion by electing to supinate more at the STJ to decrease the ground reaction force (GRF) plantar to the 1st MPJ, 2) reducing the duration of their propulsive phase slightly without further supinating the STJ during propulsion, or 3) drastically reducing the duration of their propulsive phase by pronating their STJ during propulsion.

My guess is that those feet with fairly normal STJ axis spatial location will choose option #1, those feet with more significantly medially deviated STJ axes will choose #2 or #3 due to the central nervous system choosing that particular walking style to A) reduce the pain of walking, and/or B) increase the metabolic efficiency of walking.

As far as your other question is concerned, the windlass exerts its STJ supination moment as follows:

1. Hallux dorsiflexion causes increase in tensile force medial band of central component of the plantar aponeurosis (MBCCPA).

2. Increase in tensile force in MBCCPA causes increase in posteriorly directed compression force on first metatarsal head.

3. The simultaneous occurrence of #1 and #2 cause a rearfoot dorsiflexion moment and first ray plantarflexion moment which together cause a medial longitudinal arch raising moment [the magnitude of which will be dependent on the height of the medial longitudinal arch].

4. Medial longitudinal arch raising moment and posteriorly-directed compression force on the first metatarsal, first cuneiform and navicular will cause increased posteriorly-directed compression force at talo-navicular joint which will tend to push the talus posteriorly, which is one of the components of STJ supination motion. This posterior pushing force on the talar head will be resolved into a STJ supination moment, as long as the STJ axis is not too medially deviated. If the STJ axis is extremely medially deviated, this posterior pushing force will cause a STJ pronation moment.

Hope this helps.

 

Nicely put.:drinks

 

The original question was does first met plantar flexion cause STJ supination. What I was trying to do was give an example where the met plantarflexed, but the cause of the plantarflexion was not directly acting on the metatarsal. So, met plantar flexion will tend to correlate with STJ supination because all the bones are connected together, but STJ supination is not necessarily caused by Met plantar flexion. I guess another point I wanted people to think about is what causes the met to plantarflex. If you say that met plantar flexion causes STJ supination then you have to figure out what forces cause the met to plantar flex. This is why I had a hard time with the original question. I couldn't figure out what you thought was causing the met to plantar flex.

In Kevin's comment the source of plantar flexion moment on the metatarsal is missing. Yes if you were to take your fingers and grab the metatarsal with your fingers and twisted in the direction of plantar flexion there would be an increase in ground reaction force under the metatarsal.

Other sources of plantar flexion moment on the metatarsal Include:

tension in the peroneus longus tendon and compression at the met cuneiform joint. Specifically the force couple of a posteriorly directed force from the tendon and an anteriorlly didrected push from the cuneiform acting on the metatarsal.

Tension in the plantar ligament and compression at the joint surface at the met cuneiform ligament

And compression at the 1st mpj and compression at the met cuneiform joint. (Windlass)

The windlass creates different moments at different joints.
At the STJ think about the break in the cyma line in the sagittal plane. (The cyma line was described as a radiologic finding by looking at a lateral view x-ray and drawing a line at the talonavicular joint and the calcaneocuboid joint.) With pronation there is an anterior break of the cyma line where the anterior aspect of the talar head is anterior to the calcaneocuboid joint. With a posterior break of the cyma line the talar head sits posterior to the calcaneo cuboid joint. That was the motion that occurs at the joint. Now we have to think about the forces that cause that motion.

Take a loaded foot in static stance where there is tension in the plantar fascia. The tension of the fascia pulls the proximal phalanx into the first met. The phalanx doesn't go anywhere so there must be no net ant post force. (F = ma, a = 0 ) There must be a force from the metatarsal head acting on the base of the phalanx to maintain ant post equilibrium of the prox phalanx. If there is a force from the met acting on the phalanx there must also be a force from the phalanx acting on the met. (for pictures see my windlass paper or draw them yourself as the pictures help the understanding. Draw the bones separately) The met is not moving so there must a force from the cuneiform acting on the base of the metatarsal. Repeat for all bones back to the talus. So, the supination moment from the windlass comes from an anterior pull at the fascial attachment of the calcaneus and a posterior push from the navicular acting on the talar head.

So, simultaneously the windlass causes a plantar flexion moment acting on the metatarsal and a supination moment at the STJ (in most feet)

If you were to grab the 1st toe and dorsiflex it you would increase tension in the plantar fascia. Increased tension in the fascia will cause an increase in plantar flexion moment acting on the metatarsal. So, as you grab the toe and dorsiflex it you will be increasing plantar flexion moment of the first metatarsal and supination moment at the STJ. In addition the plantar flexion moment on the metatarsal will tend to shift the center of pressure under the foot medial and this will decrease the pronation moment from the ground.

The answer to your question Robert, is in drawing out all the free body diagrams of each bone. Start with the know forces and then estimate the missing forces. I went to the local college bookstore and bought an engineering textbook on statics. I did all the problems at end of the chapters and looked at the answers at the back of the book. It took me a while to work through it. The mistake that I made when teaching was trying to get people to understand what took me more than a month to learn in about four hours of class time. Anyway if you made it all the way through this post you might find the statics textbook fun and entertaining. I found it quite useful.

It reminds me of a story a former student told me. He said he was on top of his roof fixing a TV antenna with his father and his father was having trouble rotating the antenna. My student said he thought of me when he showed his father where to grab the antenna so that it would be easier to rotate it. So, someone else found it useful too.

Cheers,

Eric

 

Hi Robert
Thank you for the welcome, this is a great blog full of interesting and thought provoking subjects. Regarding your point about a ruptured liagamnet which results in a deformed foot, is probably a challenging question as it is perhaps an extreme situation. If I could for the moment ignore the injury and talk about a somewhat normal foot, if we looked this foot print I sand. We might see that the arch of the foot is somewhat supported by the sand and that the entire plantar aspect would be supported and that possibly there would be a reduced amount of “pronation”. There are other complicating factors such as the base of the 5th metatarsal, which often comes into contact with the firm surface under foot early and therefore forces the mid and forefoot into a quicker pronation movement. So if I was to take a cast it might be better taken over a sand box with the patient partial weight bearing. Does this make any sense?

 

Re: Overpronation

Robert Stated:

Let us consider for a second how a normal healthy foot with a nice healthy function will appear in relaxed stance. The orientation of the Sub Talar Axis means the centre of mass will tend to come down on the pronation side of the line, so the foot will pronate until something stops it. What structures limit pronation? The Tibial muscles group certainly, but it would not be efficient for them to hold the patient in supination when in relaxed stance. The planter fascia / windlass? Sure but there is not a lot of tension there before heel raise (in most patients). Bony osseous limitation? Hope not, unless you are really arthritic! I contend that in most cases the limiting structure is the Deltoid ligament complex which limits the range generally. And what position will that keep the STJ in? Pretty near the maximally pronated position. It represents a position the foot CAN achieve and little more than that. It does not indicate the degree to which the calc everts during gait 2, 3 . The position of a “normal” healthy, effectively functioning foot during static weight bearing may be closer to maximally pronated than neutral, its is certainly not neutral!

DrSha Replies:
What happens when PERM is reached in stance and lets assume the deltoid, plantar fascia, etc. have reduced or eliminated the STJ from pronating further.
Are there any other structures (areas in the rearfoot) that can then supply additional “overpronation” into the foot or does all pronation exist in the STJ?
A possible example that I suggest is that once the foot has reached PERM, the medial side of the plantar pad (the soft tissue that exists from the plantar osseous calcaneal surface to the skin can collapse under the forces that exist and effectively pronate the rearfoot.
:drinks
DrSha

 

Re: Overpronation

Perhaps Admin would be kind enough to move this to the English thread on the same article...

However

This is going to take some explaining. Pronation is a movement of the STJ.

Oh and remind us what PERM is? Sorry, I tend to forget non standard acronyms.

Cheers
Robert

 

Never mind. Just remembered. Pronation end range of movement wasn't it.

 

Dennis you're back! Always a pleasure. However your first post after your hiatus and you are straight in where you left off (sigh).

Why don't we leave the PERMs to the hairdressers for now and get your thoughts on the original topic being discussed here

Ian

 

From today's Mail on Sunday:

'The medical term for our condition is hyperpronation'

 

I read your add on " the medical term for our condition is hyperpronation" and I picture you crying into your corn flakes, Robert face going red and Ella screaming something like MORON.

 

The question is, would you put your 8 year-old daughter forward for elective surgery?

 

Don't know about you but this surgery just looks wrong to me. Inserting a bolt into the mechanism to jam it up eh! sounds like a bodge job to me. Especially at the point of least mechanical advantage i.e. at the lever fulcrum where huge forces are required to resist opposite applied moments.

If your offside front car suspension unit was banging against the inner wing and instead of changing the damper/shock absorber or mainspring the mechanic jammed a bolt between the wishbone and the sub frame, I don't think you or the car would be very happy for long.

I wonder what happens at the interfaces when you run on uneven ground or jump off a low wall with this bolt inserted in the sinus tarsi.

Am I not understanding something here perhaps its a rubber trunion:wacko:

Dave Smith

 

I've started a separate thread off for this. Its not the first time this has been in the national papers, it seems to be the "next big thing."

Please comment here